Topic: Ischaemic heart disease, pulmonary embolism.
Question: How will you diagnose a suspected case of pulmonary embolism? What are the relevant investigations to be performed?
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Clinical evaluation: This includes a detailed history and physical examination focused on detecting features suggestive of PE.
History:
•Ask about any recent immobility (surgery, injury, long travel), which can predispose to VTE.
•Ask about symptoms of PE like:
›New onset dyspnea: May describe as sudden, sharp and pleuritic. Worse on exertion or when supine.
›Chest pain: Also sharp or stabbing, exacerbated by deep breathing or coughing.
›Cough: May produce frothy or blood-tinged sputum. Dry cough is also common.
›Hemoptysis: Coughing up of blood can occur with pulmonary infarction.
›Pre-syncope or syncope: Due to reduced cardiac output from pulmonary hypertension and/or oxygen desaturation.
›Orthopnea: Dyspnea that worsens when lying flat, relieved by sitting up. Due to redistribution of blood flow in supine position.
›Palpitations: May experience with pulmonary hypertension and right heart strain.
›Leg pain or swelling: Unilateral calf pain, tenderness or swelling can indicate DVT which can embolize to lungs.
Examination:
•Vital signs: Tachypnea >20 breaths/min, tachycardia, hypotension and fever may indicate hemodynamic compromise from PE. Check oxygen saturation – levels below 92% on room air are significant.
•Respiratory exam: May reveal rapid, shallow breathing with accessory muscle use. Decreased chest expansion and dullness to percussion if pleural effusion present. Crackles can be heard over infarcted areas.
•Cardiovascular: Elevated JVP, accentuated P2, right ventricular heave or palpable thrill may indicate pulmonary hypertension.
•Leg veins: Examine for calf tenderness, swelling or cord-like veins which can indicate DVT. Homans’ sign is unreliable.
•Other: Cyanosis indicates significant hypoxemia. Pleural rub may be heard with pulmonary infarction.
Risk assessment:
– Determine the patient’s risk factors for DVT and PE, including immobilization, surgery, trauma, malignancy, pregnancy, obesity, smoking, and inherited thrombophilia
– Assess the patient’s overall clinical stability, as this may impact management decisions and the need for further testing
The presence of unexplained or new symptoms and signs suggestive of PE, especially in the context of risk factors, raise the clinical suspicion and help determine which diagnostic tests may be appropriate based on the estimated pre-test probability. D-dimer, for example, has a higher negative predictive value when the pre-test probability is low. Clinical evaluation thus forms a crucial first step in diagnosing what can be a life-threatening condition if misdiagnosed or left untreated.
Relevant investigations to be performed:
•Arterial blood gas: To check for hypoxemia, hypocapnia and respiratory alkalosis which may indicate PE.
•D-dimer assay: First-line test, as concentration >500 ng/mL can indicate thrombus formation and guide need for imaging. However, it is non-specific and levels also rise in other conditions. So a negative D-dimer can exclude PE in low pre-test probability cases only.
•Chest X-ray: May show nonspecific signs like atelectasis, pleural-based opacity or elevated hemidiaphragm. Mainly done to exclude other diagnoses.
• Computed tomography pulmonary angiogram (CTPA): Is the gold standard for diagnosing PE. Findings include:
›Intraluminal thrombus: Complete occlusion of a vessel by low attenuation filling defect.
›Eccentric filling defect: Thrombus along one wall of the vessel.
›Vessel cutoff: Complete cessation of opacification of vessels at the thrombus site.
›Enlarged pulmonary artery: May indicate hemodynamically significant PE.
›Wedge-shaped pleural-based opacity: Infarcted lung parenchyma due to lack of perfusion.
› Other signs like pleural effusion, consolidation or mosaic attenuation.
•Ventilation-perfusion scan (V/Q scan): Can also diagnose PE by demonstrating mismatch in ventilation and perfusion. Non-invasive so preferred in some cases, but less sensitive and specific than CTPA.•Pulmonary angiography: Invasive but can diagnose PE with high accuracy. Reserverd when CTPA cannot be done or is inconclusive and high suspicion of PE remains.
•Echocardiography: To check for signs of pulmonary hypertension like increased pulmonary artery pressure, right heart strain or McConnell’s sign. Their presence increases likelihood of PE though echocardiography alone cannot conclusively diagnose PE.
•Leg vein ultrasonography: To check for concurrent DVT which would support the diagnosis of PE due to embolus originating from the legs. Not always possible if patient cannot be moved.
In summary, diagnosis of PE requires a combination of clinical assessment, laboratory tests and multiple imaging modalities. No single test is confirmatory and treatment may need to be started on the basis of high probability while awaiting more definitive diagnostic tests.
History | Examination | Diagnostic Probability | |
---|---|---|---|
Risk factors for VTE: Surgery, trauma, immobility, etc. | Vital signs: Tachycardia, tachypnea, hypoxemia (SpO2 <92%), hypotension | Low: No symptoms, signs or risk factors –> High negative predictive value of D-dimer |
D-dimer → If + (>500 ng/mL) proceed to imaging, if – and low probability can exclude PE |
Dyspnea (new onset, worsening, pleuritic, orthopnea) | Respiratory: Tachypnea, accessory muscle use, decreased chest expansion, crackles |
Intermediate: Risk factors +/- symptoms/signs –> D-dimer + chest imaging (CTPA or V/Q scan) |
Chest X-ray → May show atelectasis, effusion, elevated hemidiaphragm but cannot exclude or confirm PE |
Chest pain (pleuritic, worse on deep breathing/cough) | Cardiovascular: Elevated JVP, loud P2, RV heave, thrill | High: Hemodynamic instability or shock
–> High likelihood of PE, begin treatment and expedite definitive diagnosis |
CT pulmonary angiogram → Gold standard for diagnosis, shows intraluminal thrombus, vessel cutoff or enlargement |
Cough (with or without hemoptysis) | Legs: Unilateral calf swelling, tenderness, cord-like veins | Ventilation/perfusion scan → Alternative to CTPA, diagnoses PE by showing mismatch between ventilation and perfusion |
|
Pre-syncope or syncope | Other: Cyanosis, pleural rub | Pulmonary angiogram → Invasive, reserved when other tests are indeterminate or unable to be done but high suspicion remains |
|
Palpitations | Leg vein ultrasonography → Checks for concurrent DVT which increases probability of PE |
||
Unilateral leg pain or swelling | Echocardiography → Checks for signs of pulmonary hypertension like RV strain which supports diagnosis of PE |
Diagnostic Tests | Description |
---|---|
D-dimer | Blood test, if + (>500 ng/mL) proceed to imaging, if – and low probability can exclude PE |
Chest X-ray | May show atelectasis, effusion, elevated hemidiaphragm but cannot exclude or confirm PE |
CT pulmonary angiogram | Gold standard for diagnosis, shows ›Intraluminal thrombus: Complete occlusion of a vessel ›Eccentric filling defect: Thrombus along one wall of the vessel ›Vessel cutoff: Complete cessation of opacification of vessels at the thrombus site ›Enlarged pulmonary artery: May indicate hemodynamically significant PE ›Wedge-shaped pleural-based opacity: Infarcted lung parenchyma ›Other signs: Pleural effusion, consolidation or mosaic attenuation |
Ventilation-perfusion scan (V/Q scan) | Alternative to CTPA, diagnoses PE by showing mismatch between ventilation and perfusion |
Pulmonary angiogram | Invasive, reserved when other tests are indeterminate or unable to be done but high suspicion remains |
Leg vein ultrasonography | Checks for concurrent DVT which increases probability of PE |
Echocardiography | Checks for signs of pulmonary hypertension like ›Increased pulmonary artery pressure ›Right heart strain ›McConnell’s sign (right ventricular free wall hypokinesis) Their presence increases likelihood of PE though cannot conclusively diagnose PE |